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PubMed1994

Blood monocytes and spleen macrophages differentiate into microglia-like cells on monolayers of astrocytes: morphology.

Several morphological and functional properties of microglial cells, the resident immunoeffector cells of the central nervous system (CNS), differ from those of monocytes/macrophages in other tissues. Microglia are assumed to derive from myelonocytic lineage, possibly as a distinct subpopulation that diverges from a common cell line early in ontogeny, invades the CNS, proliferates, and differentiates into ameboid and then ramified microglia. We tested the hypothesis that some morphological and functional properties of microglia are induced in myelomonocytic cells by nervous tissue, specifically astrocytes. In the present in vitro studies we compared the differentiation of microglia, blood monocytes, and spleen macrophages on acellular substrates and on monolayers of astrocytes and fibroblasts. On acellular substrates, microglial cells at first acquire an ameboid morphology; later they show a few short, unbranched processes. On monolayers of pure astrocytes, microglial cells at first also differentiate into ameboid cells, but after 5 to 7 days they start to develop processes with large lamellopodial tips. These lengthen and branch continuously during the next 2 weeks in vitro, demarcating a round to oval territory around the small ellipsoid cell body. By contrast, on monolayers of fibroblasts the microglial cells develop an ameboid morphology, but do not grow the typical long branched processes of the ramified form. Blood monocytes and spleen macrophages behave indistinguishably from microglia both on acellular and cellular substrates, i.e., on astroglia they develop the ramified form, while on fibroblasts they retain the ameboid shape. When microglia, macrophages, or monocytes are cultured on coverslips on top of astrocytic monolayers, i.e., physically separated from the astroglia, but exposed to the medium conditioned by astrocytes, a significant proportion of them also develop the ramified shape. These findings indicate that the ramified shape of microglia is induced by astrocytes. Since this morphology can also be induced in blood monocytes and macrophages, we take this to be further evidence for the proposition that microglial cells are derived from the myelomonocytic lineage, and, moreover, that properties of resident macrophages are largely determined by tissue components of their host organ.

Animals↗
PubMed1986

Comparison of astrocytic morphology, proliferation, marker profile and response to neurons in wild-type and weaver mutant mouse cerebella in culture.

In serum-free monolayer cultures of early postnatal weaver (wv/wv) cerebellum granule neurons show decreased attachment, survival and neurite outgrowth when compared to wild-type (+/+) littermate cultures. wv/wv Astrocytes display a more epithelioid morphology and altered proliferation. However, both morphology and proliferation of wv/wv astrocytes were reversed to a normal phenotype by addition of purified small neurons from early postnatal cerebella from +/+ animals. Attachment of +/+ neurons to wv/wv astrocytes was not significantly different from that of +/+ astrocytes and antigenic marker profiles of wv/wv and +/+ astrocytes differed only slightly. Attempts failed to revert the abnormal wv/wv phenotype in neurons by addition of gangliosides, triiodothyronine T3, prostaglandin A2, medium containing 1% horse serum, conditioned medium from +/+ cerebellar cultures, or by cocultivation with +/+ astrocytes. We would like to suggest that the primary defect of the wv/wv mutation is predominantly an abnormality in granule cell neurons, but not of the vast majority of astrocytes.

Animals↗
PubMed1998

Amyloid-beta peptide activates cultured astrocytes: morphological alterations, cytokine induction and nitric oxide release.

A common feature of many neurodegenerative disorders is an abundance of activated glial cells (astrocytes and microglia). In Alzheimer's disease (AD), activated astrocytes are in close apposition to and surrounding the amyloid plaques. The mechanisms by which the astrocytes become activated in AD and the consequences of reactive astrocytosis to disease progression are not known. We examined the possibility that the amyloid-beta (Abeta) peptide, a major constituent of the amyloid plaque, could act as a stimulus leading to activation. We found that treatment of rat cortical astrocyte cultures with aggregated Abeta 1-42 peptide induces activation, as assessed by reactive morphological changes and upregulation of selective glial mRNA and proteins, such as the inflammatory cytokine interleukin-1beta. Abeta also stimulates inducible nitric oxide synthase (iNOS) mRNA levels and nitric oxide (NO) release. Abeta 1-42, a major form of amyloid associated with neurotoxicity, activated astrocytes in a time- and dose-dependent manner, whereas a scrambled Abeta 1-42 sequence or Abeta 17-42 had little or no effect. We also determined that the Abeta activity can be found in a supernatant fraction containing soluble Abeta oligomers. Our data suggest that Abeta plays a role in the reactive astrocytosis of AD and that the inflammatory response induced upon glial activation is a critical component of the neurodegenerative process.

Amino Acid Sequence↗
PubMedDate not supplied

[Astrocytic morphological responses in different murine brain regions in the simulation of West Nile fever].

The brains from the mice infected intraperitoneally (with development of these or those symptoms of viral encephalitis) or intramuscularly with the Astrakhan West Nile fever virus strain (AcT 986) was pathomorphologically studied. Clinicomorphological changes in the neurons and vessels of the microcirculatory bed were found in the dorsal regions of medulla oblongata. Immunohistochemicall analysis showed that mature and/or activated astrocytes increased in number, largely in the animals without clinical manifestations of encephalitis. The findings provide evidence that cerebral astrocytes play a protective and adaptive role that seems to depend on the biological properties of the pathogen.

Animals↗
PubMed1998

Morphological astrocytic changes in complicated human brain trauma. A light and electron microscopic study.

The astrocytic changes and reactivity in human brain trauma complicated with subdural haematoma or hygroma have been analysed in nine patients. Cortical biopsies of frontal, temporal and parietal regions were examined with light and transmission electron microscopy. At light microscopy level oedematous clear and dense astrocytes, binucleated and multinucleated astrocytes and hypertrophic reactive astrocytes were distinguished in either moderate or severe vasogenic brain oedema. Swollen, clear and dense perineuronal astrocytes were observed compressing and indenting dark, degenerated pyramidal and non-pyramidal nerve cells. At electron microscopy level glycogen-depleted and glycogen-rich astrocytes were found in some patients. Dense and reactive hypertrophic astrocytes exhibited increased amounts of dilated smooth endoplasmic reticulum, microtubules, lipofucsin granules, gliofilaments and alpha type glycogen particles. In severe oedema the astrocytic ensheathment of synaptic contacts is lost, the perivascular astrocyte end-feet appeared dissociated from the capillary basement membrane and the interastrocytary gap junctions are disrupted. The posttraumatic neurological deficits and the neurobehavioural disorders of the patient studied are correlated with astrocyte ultrastructural changes and blood brain barrier disruption.

Adolescent↗
PubMed1996

Whole-cell chloride currents in rat astrocytes accompany changes in cell morphology.

Astrocytes can change shape dramatically in response to increased physiological and pathological demands, yet the functional consequences of morphological change are unknown. We report the expression of Cl- currents after manipulations that alter astrocyte morphology. Whole-cell Cl- currents were elicited after (1) rounding up cells by brief exposure to trypsin; (2) converting cells from a flat polygonal to a process-bearing (stellate) morphology by exposure to serum-free Ringer's solution; and (3) swelling cells by exposure to hypo-osmotic solution. Zero-current potentials approximated the Nernst for Cl-, and rectification usually followed that predicted by the constant-field equation. We observed heterogeneity in the activation and inactivation kinetics, as well as in the relative degree of outward versus inward rectification. Cl- conductances were inhibited by 4, 4-diisothiocyanostilbene-2,2'-disulfonic acid (200 microM) and by Zn2+ (1 mM). Whole-cell Cl- currents were not expressed in cells without structural change. We investigated whether changes in cytoskeletal actin accompanying changes in astrocytic morphology play a role in the induction of shape-dependent Cl- currents. Cytochalasins, which disrupt actin polymers by enhancing actin-ATP hydrolysis, elicited whole-cell Cl- conductances in flat, polygonal astrocytes. In stellate cells, elevated intracellular Ca2+ (2 microM), which can depolymerize actin, enhanced Cl- currents, and high intracellular ATP (5 mM), required for repolymerization, reduced Cl- currents. Modulation of Cl- current by Ca2+ and ATP was blocked by concurrent whole-cell dialysis with phalloidin and DNase, respectively. Phalloidin stabilizes actin polymers and DNase inhibits actin polymerization. Dialysis with phalloidin also prevented hypo-osmotically activated Cl- currents. These results demonstrate how the expression of astrocyte Cl- currents can be dependent on cell morphology, the structure of actin, Ca2+ homeostasis, and metabolism.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2006

The impact of astrocytic gap junctional coupling on potassium buffering in the hippocampus.

Astrocytic gap junctions have been suggested to contribute to spatial buffering of potassium in the brain. Direct evidence has been difficult to gather because of the lack of astrocyte-specific gap junction blockers. We obtained mice with coupling-deficient astrocytes by crossing conditional connexin43-deficient mice with connexin30(-/-) mice. Similar to wild-type astrocytes, genetically uncoupled hippocampal astrocytes displayed negative resting membrane potentials, time- and voltage-independent whole-cell currents, and typical astrocyte morphologies. Astrocyte densities were also unchanged. Using potassium-selective microelectrodes, we assessed changes in potassium buffering in hippocampal slices of mice with coupling-deficient astrocytes. We demonstrate that astrocytic gap junctions accelerate potassium clearance, limit potassium accumulation during synchronized neuronal firing, and aid in radial potassium relocation in the stratum lacunosum moleculare. Furthermore, slices of mice with coupling-deficient astrocytes displayed a reduced threshold for the generation of epileptiform events. However, it was evident that radial relocation of potassium in the stratum radiatum was not dependent on gap junctional coupling. We suggest that the perpendicular array of individual astrocytes in the stratum radiatum makes these cells ideally suited for spatial buffering of potassium released by pyramidal cells, independent of gap junctions. In general, a surprisingly large capacity for K+ clearance was conserved in mice with coupling-deficient astrocytes, indicating that gap junction-dependent processes only partially account for K+ buffering in the hippocampus.

Animals↗
PubMed1993

Glia cells of the monkey retina. I. Astrocytes.

Morphology and distribution of retinal astrocytes have been studied in macaque monkeys by immunocytochemical localization of glial fibrillary acidic protein (GFAP). With the exception of the fovea and the far periphery, astrocytes are ubiquitous in the nerve fiber layer (NFL) and the ganglion cell layer (GCL) of the monkey retina. The morphology of NFL astrocytes changes gradually, from star-shaped in the periphery to bipolar close to the optic disc. By contrast, GCL astrocytes maintain their star-shaped appearance throughout the retina. Astrocytes are unevenly distributed in the monkey retina, showing the highest concentration around the optic disc, and particularly low densities in the perifoveal region and the far periphery. The fovea proper is devoid of astrocytes. Employing high-resolution confocal microscopy, we could demonstrate that astrocytes form manifold contacts to blood vessels. In addition, bundles of NFL astrocyte processes are co-localized with axon bundles, individual astrocytes forming contacts to several axon bundles. In contrast, a similar affinity of astrocytes to ganglion cell somata was never observed. Thus, our data confirm and extend the current knowledge of morphology and putative function of astrocytes in mammalian and especially the primate retina.

Animals↗
PubMed1984

Astrocytic membrane morphology: differences between mammalian and amphibian astrocytes after axotomy.

Previous studies have shown that astrocytes in some nonmammalian species provide a favorable environment for axonal elongation, whereas mammalian astrocytes are thought to inhibit fiber outgrowth. The present study was performed to determine whether any plasma membrane differences exist between these glial elements which could account for their contrasting effects upon axonal outgrowth. Astrocytic scars were formed in optic nerves of rats, newts, and frogs by enucleation. Subsequently, the astrocytic membranes were examined with the freeze-fracture technique. Orthogonal arrays of small intramembranous particles (IMPs) are a prominent component of the plasma membranes of normal mammalian astrocytes; these arrays are most numerous in astrocytic membranes that form an interface between the CNS and nonneural tissue. Astrocytic membranes within the normal CNS parenchyma, however, possess much lower densities of arrays. Following axotomy and Wallerian degeneration, the density of arrays increased threefold within the parenchyma of the optic nerve, while remaining constant at the glia limitans. In striking contrast, only a few aggregates of IMPs that resembled orthogonal arrays could be found in normal and reactive astrocytes of amphibians, although the cytology of these glial cells and density of the scars are otherwise similar to those of their mammalian counterparts. These findings suggest (1) that a proliferation of orthogonal arrays in astrocytic plasma membranes is a prominent feature of gliosis in the mammalian CNS and (2) that differences in the composition of reactive mammalian and amphibian astrocytic membranes may account for variations in axonal-glial interactions within the injured CNS.

Aging↗
PubMed2026

Astrocyte reactivity by alcohol dependence in the central amygdala.

Astrocytes play essential roles in maintaining brain homeostasis and in contributing to synaptic functions, but, in response to injury, infection, or disease, astrocytes can downregulate their homeostatic and physiological functions while increasing neuroinflammatory responses. The central amygdala (CeA) is important for stress responsivity and the development of alcohol (ethanol) dependence. Using a multi-omics approach in Aldh1l1-EGFP/Rpl10a mice and the chronic intermittent ethanol two-bottle choice (CIE-2BC) model, we have characterized the translational response of CeA astrocytes, as well as the proteomic and phosphoproteomic changes in ethanol dependent, non-dependent, and naïve mice. We identified astrocyte-specific alterations in neuroimmune functions and antioxidant/oxidative stress pathways in ethanol dependent mice as well as cytoskeletal plasticity related pathways in non-dependent mice. Proteomic analysis showed down-regulation of astrocyte physiological functions in dependent animals while phosphoproteomic analysis identified pathways associated with cytoskeleton remodeling in both dependent and non-dependent mice. Reconstructions of astrocyte morphologies demonstrated increased CeA astrocyte complexity in dependent and non-dependent groups compared to naïve mice. The astrocyte-specific activation of neuroimmune and antioxidant pathways, down-regulation of homeostatic functions, alteration in protein phosphorylation-mediated cytoskeleton remodeling, and increased astrocyte morphological complexity demonstrate that ethanol dependence induces astrocyte reactivity in the CeA consistent with both adaptive and maladaptive changes. These findings highlight the role of CeA astrocytes in the progression from alcohol intake to dependence and represent a first step toward identifying astrocyte-specific therapeutic strategies to treat Alcohol Use Disorder (AUD) aimed at potentiating reactive astrocyte adaptive changes and inhibiting maladaptive responses.

Animals↗
PubMed2006

Synaptic plasticity, astrocytes and morphological homeostasis.

Recent discoveries suggest that astrocytes are an integral part of synaptic connections, as they sense and modulate synaptic activity. Moreover, there is evidence that astrocytes change the number of synaptic connections directly via synaptogenic signals or indirectly, by modifying the morphology of axons and dendrites. Here, we formulate the hypothesis that astrocytes mediate the morphological homeostasis of nerve cells, which is any adaptation of the morphology of a neuron to preserve its ability to respond to and generate synaptic activity during learning and memory-induced changes. We argue that astrocytes control neuronal morphology locally and across long-ranging assemblies of neurons and that on the other hand, astrocytes are part of the engram with plasticity-related changes affecting their morphology.

Animals↗
PubMed2004

Evidence that the branched-chain alpha-keto acids accumulating in maple syrup urine disease induce morphological alterations and death in cultured astrocytes from rat cerebral cortex.

Severe neurological symptoms, cerebral edema, and atrophy are common features of the inherited metabolic disorder maple syrup urine disease (MSUD). However, the pathomechanisms involved in the neuropathology of this disease are not well established. In this study, we investigated the effects of the branched-chain keto acids (BCKA) alpha-ketoisocaproic (KIC), alpha-ketoisovaleric (KIV), and alpha-keto-beta-methylvaleric (KMV), which accumulate in MSUD, on astrocyte morphology and cytoskeleton reorganization. Cultured astrocytes from cerebral cortex of neonatal rats were exposed to various concentrations of the BCKA and cell morphology was studied. We observed that these cells changed their usual polygonal morphology when exposed to BCKA, leading to the appearance of fusiform or process-bearing cells. Furthermore, longer exposures to the BCKA elicited cell death at all concentrations studied, attaining massive death at the highest concentrations. Immunocytochemistry with anti-actin or anti-GFAP antibodies revealed that the BCKA induced reorganization of actin and GFAP cytoskeleton. In addition, astrocytes treated with lysophosphatidic acid, an upstream activator of the RhoA GTPase pathway, totally prevented the morphological alterations and cytoskeletal reorganization induced by KIV, indicating that this effect could be mediated by the RhoA signaling pathway. Furthermore, the effects of BCKA on astrocyte morphology were prevented by creatine. In addition, creatine kinase activity was inhibited by KIC and KIV; this inhibition was prevented by creatine, indicating that these keto acids compromise brain energy metabolism. Considering that astroglial cells are critical to brain development and functioning, it is conceivable that alterations of the actin network by BCKA may have important implications in astrocytic function and possibly in the pathogenesis of the neurological dysfunction and brain damage of MSUD patients.

Actins↗
PubMed1994

Three-dimensional morphology of astrocytes and oligodendrocytes in the intact mouse optic nerve.

The three-dimensional morphology of astrocytes and oligodendrocytes was analysed in the isolated intact mature mouse optic nerve, by correlating laser scanning confocal microscopy and camera lucida drawings of single cells, dye-filled with lysinated rhodamine dextran or horseradish peroxidase, respectively. These techniques enabled the entire process field of single dye-filled cells to be visualized in all planes and resolved the fine details of glial morphology. Morphometric analysis showed that the processes of all astrocytes had branches ending at the pial surface, on blood vessels, and freely in the nerve; branches ending in the nerve were described to end at nodes of Ranvier in the accompanying paper. Astrocytes were classified into a single morphological population in which each cell subserved multiple functions. The results of this study do not support the contention that astrocytes can be subdivided into two morphological and functional subtypes, namely type-1 and type-2, which have process ending either at the glia limitans or at nodes, respectively. Three-dimensional analysis of oligodendrocyte units, defined as the oligodendrocyte, its processes and the axons it ensheaths, showed the provision of single myelin segments for an average of 19 nearby axons (range 12-35) with a mean internodal length of 138 microns (range 50-350 microns). Mouse optic nerve oligodendrocytes were a homogeneous population and were markedly similar to those in the rat optic nerve. The results of our analysis of oligodendrocyte morphology are consistent with the view that the number and internodal length of myelin sheaths supported by a single oligodendrocyte are related to the diameter of the ensheathed axons.

Animals↗
PubMed1996

Stimulation of glutamine synthetase activity by excitatory amino acids in astrocyte cultures derived from aged mouse cerebral hemispheres may be associated with non-N-methyl-D-aspartate receptor activation.

We have been using glial cells derived from aged mouse cerebral hemispheres (MACH) at several passages to study the responsiveness of astrocytes to microenvironmental signals in culture. In the present study, we examined the effects of excitatory amino acids on the activity of glutamine synthetase, a marker for astrocytes. MACH glia cell passages 25 to 29 were used. Culture groups were Dulbecco's modified Eagle's medium +10% fetal bovine serum (control); glutamate 100 microM; gamma-amino-3-hydroxy-5-methyl isoxazole-4-propionic acid (AMPA) 50 microM; kainic acid 10 microM; N-methyl-D-aspartate (NMDA) 10 microM. In all treated groups glutamine synthetase activity was significantly higher than in controls. We speculate that this increase represents an enhanced differentiation of immature astrocytes. In a second series, we examined the effects of glutamate receptor antagonists on glutamine synthetase activity as follows. MACH cultures were treated with glutamate 100 microM in combinations with either L(+)-2-amino-3-phosphonopropionic acid (L-AP3; 50 microM); D(-)-2-amino-5-phosphonopentanoic acid (D-AP5; 50 microM) or 6,7-dinitroquinoxaline-2,3-dione (DNQX, 50 microM). The increase in GS activity produced by glutamate was inhibited by the non-selective NMDA receptor antagonist, DNQX, but not by the metabotropic receptor antagonist, L-AP3 or a selective NMDA receptor antagonist, D-AP5. We also found that in cultures treated with glutamate, a number of astrocytes resembled "reactive astrocytes" morphologically. These astrocytes were absent in cultures treated with glutamate+DNQX. The findings provide supportive evidence that astrocytes from aged mouse cerebral hemispheres respond to excitatory amino acids and that this response is mediated by non-NMDA receptor activation.

2-Amino-5-phosphonovalerate↗
PubMed1993

Morphology of astrocytes and oligodendrocytes during development in the intact rat optic nerve.

The detailed three-dimensional morphology of macroglial cells was determined throughout postnatal development in the intact rat optic nerve, a central nervous system white matter tract. Over 750 cells were analyzed by intracellular injection of horseradish peroxidase or Lucifer Yellow to provide a new perspective of glial differentiation in situ. Retrograde analysis of changes in glial morphology allowed us to identify developmental timetables for three morphological subclasses of astrocytes and oligodendrocytes, and to estimate their time of emergence from undifferentiated glial progenitors. Glial progenitors were recognised throughout postnatal development and persisted in 35-day-old nerves, where we suggest they represent adult progenitor cells. Astrocytes were present at birth, but the majority of these cells developed over the first week as three morphological classes emerged having either transverse, random, or longitudinal process orientation. Several lines of evidence led us to believe that the majority of astrocytes in the rat optic nerve were morphological variations of a single cell type. Young oligodendrocytes were first observed 2 days after birth, indicating that they diverged from progenitors at or near this time. During early development these cells extended a large number of fine processes, which then bifurcated and extended along axons. Later, as myelination proceeded, oligodendrocytes exhibited fewer processes which grew symmetrically and uniformly along the axons, resulting in a highly stereotypic mature oligodendrocyte form. Our analysis of oligodendrocyte growth suggests that these cells did not myelinate axons in a random manner and that axons may influence the myelinating processes of nearby oligodendrocytes.

Animals↗
PubMed1987

Synergistic action of thyroid hormone, insulin and hydrocortisone on astrocyte differentiation.

We report here on the synergistic regulation of astrocyte development by 3 hormones: thyroid hormone (TH), insulin, and hydrocortisone (HC). Their effect, in a defined serum-free media, on astrocyte morphology, on glia fibrillary acidic protein (GFAP) immunostaining pattern, and on glutamine synthetase (GS) was investigated. TH transformed the flat, polygonal astrocytes into process-bearing cells. This effect was accentuated by insulin, which by itself had no effect on astrocyte morphology. The morphological transformations were accompanied by changes in the pattern of GFAP immunostaining which indicated a more organized and directed cytoskeleton arrangement in the TH-insulin treated cultures. Over 95% of the cells in the culture expressed GFAP. All 3 hormones regulated GS levels. TH increased GS levels by 50% and insulin raised its levels by 3-fold. While having no effect on astrocyte morphology, HC increased GS levels by 3.7-fold in both the hormone-free and insulin-supplemented medium. HC acted synergistically with insulin in its action on GS bringing about a 12-fold increase in the enzyme activity. In contrast, TH did not interact with insulin and was additive with HC in its action on GS. The continuous presence of insulin and TH was required to maintain their morphological and GS effect, suggesting that these hormones might not only be important for astrocyte differentiation, but later on for astrocyte function as well. Since astrocytes interact with and affect neurons and oligodendrocytes, the findings reported here might have bearing on the development and function of these other brain cells as well.

Animals↗
PubMed1981

Responsiveness of fetal rat brain cells to glia maturation factor during neoplastic transformation in cell culture.

The effect of partially purified extracts from adult pig brains containing a glia maturation protein factor (BE) has been investigated on neural cells during carcinogenesis. Pregnant BD IX-rats were given a single transplacental dose of the carcinogen ethylnitrosourea (EtNU) on the 18th day of gestation. The brains of the treated fetuses were transferred to cell culture and underwent neoplastic transformation with a characteristic sequence of phenotypic alterations which could be divided into five different stages. During the first 40 days after explantation (stage I & II) BE induced morphological differentiation of epitheloid neural cells into astrocytes. This occurred in carcinogen treated cells as well as in untreated control cultures. At the same time cells with astrocyte morphology showed accumulation of glial fibrillary acidic protein (GFA) as tested by indirect immunofluorescence with monospecific antibodies against GFA. Thereafter, in the EtNU pre-treated cultures an increased number of cells with astrocyte morphology was seen, and BE further increased the number of cells with long cytoplasmic processes. Control cells were GFA negative, while some few strongly, as well as many weakly, positive cells were seen after treatment with BE (stage III). At the later stages of neoplastic transformation the effect of BE became gradually less, and in tumourigenic cells which occurred after about 200-300 days, only a slight morphological change took place in a few cell lines. No appreciable effect on GFA-content was seen any longer, although some few weakly GFA positive cells could be observed in all permanent cell lines. Fetal rat brain cells therefore seem to become less responsive to this differentiation inducer during neoplastic transformation in cell culture.

Animals↗